An implantable medical device (IMD) is implanted in a patient to monitor, among other things, electrical activity of a heart and to deliver appropriate electrical therapy, as required. IMDs include pacemakers, cardioverters, defibrillators, implantable cardioverter defibrillators (ICD), and the like. The electrical therapy produced by an IMD may include pacing pulses, cardioverting pulses, and/or defibrillator pulses to reverse arrhythmias (e.g., tachycardias and bradycardias) or to stimulate the contraction of cardiac tissue (e.g., cardiac pacing) to return the heart to its normal sinus rhythm. IMDs sense cardiac signals of the heart to determine if and when to apply stimulus pulses.
Ventricular tachycardia (VT) is a cardiac event where the ventricles of the heart contract at an advanced rate. VT events begin in one or both ventricles of the heart. VT events are life-threatening arrhythmias that may develop into ventricular fibrillation, asystole, or sudden death. Ablation procedures may be applied to the heart to treat VT. For example, areas of the myocardium may be exposed to radiofrequency energy that is delivered to the myocardium through a percutaneous catheter. During ablation, the radiofrequency energy is applied to the strategic or predetermined locations along the ventricular myocardium. Ablation may prevent future VT events or reduce the frequency of future VT events.
During an ablation procedure, the physician must first determine the area to ablate. To identify the area to ablate, the physician induces a VT event. The physician attempts to induce a VT event that is similar to previous clinical VT events of the patient and then ablate the sections of the ventricular myocardium that manifest or sustain the induced VT events. The ablated myocardium will not be able to manifest or sustain future clinical VT events. A clinical VT event represents a VT event that occurs outside of a medical facility, or a VT event that occurs without any provocative maneuver, such as a VT event that is not induced by delivering stimulus pulses to the heart.
However, existing ablation procedures have certain limitations. In the electrophysiology (EP) lab where the ablation procedure is performed, the induced VT event may not be similar to the clinical VT event. For example, the induced VT event may have different rotor pathways and/or focal trigger locations when compared to previous clinical VT events. The physician may not know if the induced VT event is the same as or similar to the previous clinical VT events. If the induced VT event is dissimilar from the previous clinical VT events, then the induced VT event may lead to identification of a non-clinically relevant area to ablate. The non-clinically relevant area may not be involved with previous clinical VT events. Hence, the ablation procedure may not be successful in preventing future clinical VT events.
A need exists for methods and systems that provide physicians who apply ablation procedures with additional information that indicates whether an induced VT event is the same as or similar to previous clinical VT events. Such information may be useful in ensuring that an ablation procedure is applied to the correct regions of the heart to prevent future clinical VT events.